"Salt-sensitive" hypertensive patients cannot excrete sodium "loads" as readily as those with "non-salt-sensitive" hypertension. The increment of retained sodium, with a corresponding increase in blood volume, leads to an increase in cardiac output as measured by echocardiography, and is associated with a greater rise of blood pressure in salt-sensitive patients. The mechanism by which dietary sodium influences blood pressure in the two groups is not related to changes in plasma renin activity or aldosterone with salt loads, but may be due to that of the response of autonomic nervous system to these loads; in non-salt-sensitive patients autonomic "drive" may be more easily lowered by salt-loads, as compared with salt-sensitive patients in whom the persistence of such drive contributes to the rise of blood pressure.